1. Effects of autonomic balance and fluid and electrolyte changes on cardiac function in infarcted rats: A serial study of sexual dimorphism.
- Author
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Souza, NS, Dos‐Santos, RC, Silveira, Anderson Luiz Bezerra da, R, Sonoda‐Côrtes, Gantus, Michel Alexandre Villani, Fortes, FS, and Olivares, Emerson Lopes
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ELECTROLYTES , *LABORATORY rats , *MYOCARDIAL infarction , *AUTONOMIC nervous system ,SEX differences (Biology) - Abstract
Premenopausal women are known to show lower incidence of cardiovascular disease than men. During myocardial infarction ( MI), homeostatic responses are activated, including the sympathetic autonomic nervous system and the rennin-angiotensin-aldosterone system, which is related to the fluid and electrolyte balance, both aiming to maintain cardiac output. This study sought to perform a serial evaluation of sexual dimorphism in cardiac autonomic control and fluid and electrolyte balance during the development of MI-induced heart failure in rats. Experimental MI was induced in male (M) and female (F) adult (7-9 weeks of age) Wistar rats. The animals were placed in metabolic cages to assess fluid intake and urine volume 1 and 4 weeks after inducing MI (male myocardial infarction ( MMI) and female myocardial infarction ( FMI) groups). They subsequently underwent echocardiographic evaluation and spectral analysis of heart rate variability. After completing each protocol, the animals were killed for postmortem evaluation and histology. The MMI group showed earlier and more intense cardiac morphological and functional changes than the FMI group, although the extent of MI did not differ between groups ( P > 0.05). The MMI group showed higher sympathetic modulation and sodium and water retention than the FMI group ( P < 0.05), which may partly explain both the echocardiographic and pathological findings. Females subjected to infarction seem to show attenuation of sympathetic modulation, more favourable fluid and electrolyte balances, and better preserved cardiac function compared to males subjected to the same infarction model. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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